RESUMEN
Genetic factors play an important role in determining the susceptibility to ischemic stroke. Herein, we examined the association of an aldehyde dehydrogenase 2 (ALDH2) gene polymorphism with cerebral infarction. Patients with cerebral infarction (n = 963) and healthy controls (n = 921) were included. Genotyping was performed using gene chip platform analysis, and Sanger sequencing was used to confirm ALDH2 genotypes. The risk prediction of ALDH2 polymorphisms for cerebral infarction was examined under three genetic modes of inheritance. For males, ALDH2*2/*2 genotype was a significant risk factor for cerebral infarction in the co-dominant model (age-, smoking-, and drinking-adjusted OR 1.514, 95% CI 1.005-2.282, p = 0.047) and the recessive model (age-, smoking-, and drinking-adjusted OR 1.601, 95% CI 1.078-2.379, p = 0.020). However, for females, ALDH2*2/*2 genotype was a protective factor for cerebral infarction in the co-dominant model (age-, smoking-, and drinking-adjusted OR 0.450 95% CI 0.215-0.941, p = 0.034) and the recessive model (age-, smoking-, and drinking-adjusted OR 0.440, 95% CI 0.214-0.903, p = 0.025). Further, logistic regression analysis revealed that age, smoking, hypertension, hyperlipidemia, and hypercholesterolemia were significant risks for the presence of cerebral infarction. In conclusion, these findings support an association of ALDH2 gene polymorphisms with ischemic stroke in a Chinese Hakka population. In particular, homozygote ALDH2*2/*2 may be a risk factor for cerebral infarction in males, but contribute to reduced risk for cerebral infarction in females.
Asunto(s)
Aldehído Deshidrogenasa Mitocondrial/genética , Infarto Cerebral/genética , Adulto , Anciano , Anciano de 80 o más Años , Estudios de Casos y Controles , Infarto Cerebral/epidemiología , China , Femenino , Predisposición Genética a la Enfermedad , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo Genético , Estudios RetrospectivosRESUMEN
OBJECTIVE: To study the effect of electrophysiological characterization and radiofrequency ablation on idiopathic right ventricular tachycardia. METHODS: Five patients ( 3 male and 2 female ) with an average age of 35.2+/-11.2 years were enrolled in this study. 7F EPT electrode in temperature-controlled mode was used for the ablation. The temperature and power were controlled within the range of 50-55 degrees Celsius; and 30-35 W respectively. The ablation target was the point that evidently induced P-potential at posterior right ventricular septum by scaling test. Tachycardia was stopped within 3 s. Consolidated discharge was within 40 s. The ablation was ended when the tachycardia could not be evoked during routine intracardiac electrophysiology test. Aspirin (0.1 g/d) was given orally for 1 month after operation. RESULTS: The body surface electrocardiogram did not change significantly after ablation. Neither S1S1 and program med stimulation, nor intravenous drip of isoproterenol after operation evoked tachycardia. Neither tachycardia nor complication appeared 4-6 months after the test. CONCLUSIONS: (1) Posterior right interventricular septum can also give rise to idiopathic ventricular tachycardia similar to left posterior interventricular septum. Ablation at the point where P-potential can be evidently induced by scaling test could easily acquire success. (2) Idiopathic right ventricular tachycardia has typical body surface electrocardiogram when tachycardia attacks. (3) Ventricular tachycardia is different from bundle branch reciprocal ventricular tachycardia.